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On the Importance of Monitoring Blood Sugar and Other “Vital Signs”
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
The main risk factor for uric acid nephrolithiasis in patients with Type 2 diabetes was found to be low urine pH (Cameron, Maalouf, Adams-Huet et al. 2006). We are cautioned again in a subsequent report in the Clinical Journal of the American Society of Nephrology that the overly acidic urine in patients with Type 2 diabetes persists after controlling for dietary factors, body size, and age. The lower pH is due to a combination of greater net acid excretion and lower levels of ammonia buffers in patients with diabetes, which predisposes them to uric acid urolithiasis (Maalouf, Cameron, Moe et al. 2010).
Metabolic and endocrine bone disorders
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Several other dietary factors have been suggested to influence bone metabolism. Low vitamin K intake has been suggested as a risk factor for low BMD and osteoporosis, possibly by virtue of its involvement in osteocalcin metabolism. High protein and other diets associated with relatively high acid production (as quantified by renal net acid excretion) may adversely influence bone metabolism, consistent with the fact that acidosis stimulates bone resorption.
Sulfate and acid-base balance
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2023
Troels Ring, Sebastian Frische, Stephen Edward Rees, Jette Nybo, Søren Risom Kristensen
An obvious problem for this interpretation is how to understand the reported tendency of sulfate excretion to approach the traditional renal net acid excretion (NAE), i.e. urine titratable acidity plus ammonium minus bicarbonate [6]. We have previously expressed reservation with regard to the conventional whole-body model [5] for acid-base homeostasis, within which NAE is a crucial component, since it predicts urine charge to be a function of acid balance [20], which we know is wrong since charge must be zero. To develop this conundrum, we will have to advance a comprehensive whole-body model based on charge-balance to compare in theory and practice with the conventional model [5]. This is, however, not the issue here, so we have focused on analyzing the acid-base effects of sulfate excretion on the basis of charge-balance modeling alone.
Diabetes is a risk factor for high-dose methotrexate-associated AKI in lymphoma patients
Published in Renal Failure, 2020
Yujia Wang, Li Wei, Yi Guan, Qian Wang, Qionghong Xie, Chuanming Hao
Consistent with a large number of previous studies, MTX elimination and urine acidity were also risk factors of renal toxicities induced by HDMTX [5,6]. Therefore, daily monitoring of MTX concentration and sufficient use of sodium bicarbonate to achieve alkaline urine during HDMTX treatment is needed in clinical practice. In diabetic patients, we found serum MTX concentrations were significantly higher and urine pH value was lower at 0 and 24 h after MTX administration despite lower MTX dose and aggressive urine alkalinization. Lower urine pH value was observed in diabetic patients in other studies focused on nephrolithiasis, which showed that T2D patients had higher net acid excretion (NAE) and lower proportion of NAE as NH4+ measured in urine, suggesting impaired renal ammonium production and excretion in diabetes [30–32]. The mechanism remains uncertain although some animal and cell models tried to explain it with lipid accumulation in renal tubular cells as a result of T2D [33,34]. Acidic urine decreases the solubility of MTX and its metabolites and promotes the formation of crystals within renal tubules, which causes delayed MTX elimination [6]. In our study, multivariate regression analysis showed diabetes was an independent risk factor of AKI, while urine pH value not, suggesting lower urine pH value was possibly a result of diabetes.
Hyperchloremic metabolic acidosis in the kidney transplant patient
Published in Postgraduate Medicine, 2019
Debora Avila-Poletti, Leticia De Azevedo, Candela Iommi, Kristian Heldal, Carlos G. Musso
• Excessive phosphaturia [3]: It has been documented that more than 90% of transplant recipients exhibit inappropriate phosphaturia during the first months post-transplant. Moreover, metabolic acidosis is associated with an increase in urinary phosphate loss, since metabolic acidosis induces phosphaturia by impairing renal proximal tubular apical sodium gradient-dependent phosphate transporter activity. It is worth pointing out that phosphaturia induced by metabolic acidosis is independent of endogenous parathyroid hormone activity. In metabolic acidosis the increase in urinary phosphate may contribute substantially to renal proton secretion by increasing titratable acidity. Thus, phosphaturia can compensate the impaired renal net acid excretion in transplant patients. However, this hyperphosphaturia can also lead to muscle phosphorous depletion.